AD大鼠模型的制备及行为学和超微结构研究  

Establishment of Alzheimer disease rat model and its praxiology and ultrastructure research

作　　者：徐海伟[1] 黎海蒂[1] 范晓棠[2] 曹娟[1] 龚发云[1] 

机构地区：[1]第三军医大学生理学教研室,重庆400038 [2]第三军医大学神经生物学教研室,重庆400038

出　　处：《中国行为医学科学》2003年第2期123-124,127,共3页Chinese Journal of Behavioral Medical Science

基　　金：国家自然科学基金资助项目( 30 10 0 0 87);全军"十五"青年基金资助项目 ( 0 1Q0 99)

摘　　要：目的　观察大鼠皮下长期间断性注射叠氮钠后的学习记忆、中枢神经系统 β 淀粉样蛋白 (Aβ)含量和神经元超微结构的改变。方法　采用Morris水迷宫、放射免疫和透射电镜的方法。结果　注射氮钠后 4周 ,大鼠Morris水迷宫试验逃逸潜伏期明显延长 ,海马和额叶大脑皮层内Aβ含量显著升高 ,神经元内出现脂褐素沉积、髓鞘样变等退行性变 ,线粒体肿胀、嵴断裂、数目减少 ,突触小泡数目减少。结论　长期皮下注射叠氮钠可以制备AD氧化应激大鼠模型 ,并导致中枢Aβ的升高 。Objective To observe the learning and memory, level of β amyloid protein and ultra structure changes in the central nervous system of the rats which were chronically injected sodium azide . Methods After the establishment of AD model, the memory of the rats was surveyed by Morris water maze test, the level of Aβ was assayed with radioimmunoassay and the ultrastructure of neuron was observed with transmission electron microscope. Results Increase of escape latency in Morris water maze test and elevation of β amyloid protein level in the frontal cortex and hippocampus of rats were obvious after injection of sodium azide. And the ultra structure of neuron including retrograde degeneration such as lipofuscin deposit and myelin sheath like changes, mitochondria swelling and cristae fragmentation, synaptic corpuscle decreased. Conclusion An Alzheimer disease rat model was established by chronically subcutaneously injection of sodium azide, which resulted in increasing of β amyloid protein level in the central nervous system , retrograde degeneration and mitochondria damage in the neurons.

关 键 词：阿尔茨海默氏病 氧化应激 学习记忆 Β-淀粉样蛋白 大鼠 

分 类 号：R749.16[医药卫生—神经病学与精神病学] R338.64[医药卫生—临床医学]